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71.
Patients with dilated stenoses and recanalized occlusions were evaluated to assess the initial and long-term results of percutaneous transluminal angioplasty (PTA) in the femoropopliteal artery. The follow-up period was at least 1 year. The initial success rate was 84% (128/164). The initial results were influenced by the radiologist's experience, catheter selection, and type of lesion. The 5- and 7-year cumulative patency rates were 70% and 60%. There was no difference in long-term patency between initially successful stenoses and short (less than 3 cm) occlusions. Both the morphology and location of the stenotic lesion influenced the long-term results. Although many factors influence the initial and long-term success rate, results of this study justify PTA in the femoropopliteal artery. Patients with localized stenoses and short occlusions are best suited for this treatment.  相似文献   
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2010年8月,美国心脏病学会基金会(ACCF)、美国心脏学会(AHA)共同发布了美国食品药品管理局(FDA)关于氯吡格雷的"盒装警告",主要针对医师和患者提出建议,其内容包括:通过检测药物基因型以明确患者氯吡格雷的代谢变化,患者不良反应的风险,基因多态性对氯吡格雷的代谢及临床影响。  相似文献   
76.

Purpose  

18F-Fluoride PET/CT is a relatively undervalued diagnostic test to measure bone metabolism in bone diseases. Hyperostosis cranialis interna (HCI) is a (hereditary) bone disease characterised by endosteal hyperostosis and osteosclerosis of the skull and the skull base. Bone overgrowth causes entrapment and dysfunction of several cranial nerves. The aim of this study is to compare standardised uptake values (SUVs) at different sites in order to quantify bone metabolism in the affected anatomical regions in HCI patients.  相似文献   
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目的:中性粒细胞粘附在缺血再灌注损伤中有非常重要的作用。本文用SD大鼠趾长屈肌缺血再灌注损伤模型,观察L一粘附素单抗LAM1—116在缺血再灌注损伤中的作用。方法:30只SD大鼠被均分为2组:LAM1—116组和生理盐水对照组。每只大鼠的一侧趾长屈肌作为正常对照,另外一侧进行 3 h缺血 4 h再灌注。结果:LAM1— 116组实验侧的髓过氧化物酶为正常的2倍(2.3±2.2),生理盐水对照组则为正常的28倍(27.5±11.7)(P<0.001);LAM1—116组的湿重比(1.10± 0.10)、疲劳肌力(77. 1%±12.1%)与对照组相比(分别为 1. 23± 0. 10和 49. 7%± 9 .3%)明显改善(P< 0.05);组织学上,LAM1—116组的中性粒细胞局部浸润显著减少,水肿减轻。结论:通过 L-粘附素单克隆抗体 LAM1— 116阻断 L-粘附素的功能,可以有效地降低中性粒细胞在再灌注肌肉中的浸润,防止组织水肿,从而改善肌肉的功能。  相似文献   
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Yan  Z; Zhang  J; Holt  JC; Stewart  GJ; Niewiarowski  S; Poncz  M 《Blood》1994,84(7):2329-2339
Using recombinantly expressed proteins and synthetic peptides, we examined the structural/functional features of the platelet chemokines, neutrophil-activating peptide-2 (NAP-2) and platelet factor 4 (PF4); that were important in their activation of neutrophils. Previous studies with the chemokine interleukin-8 (IL-8) had shown that the N- terminal region preceding the first cysteine residue was critical in defining neutrophil-activating properties. We examined whether NAP-2 and PF4 had similar structural requirements. In the Ale-glu-leu-arg (AELR) N-terminus of NAP-2, substitution of E or R abolished Ca2+ mobilization and elastase secretion. Unlike the parent molecule PF4, AELR/PF4, the hybrid formed by replacing the N-terminal sequence of PF4 before the first cysteine residue with the homologous sequence of NAP- 2, stimulated Ca2+ mobilization and elastase secretion. Furthermore, the effect of amino acid substitutions in the ELR motif differed from those seen with NAP-2 in that conserved substitutions of E or R in NAP- 2 abolished activity, but only reduced neutrophil activation in the hybrid. These studies show that just as with IL-8, the N-termini of NAP- 2 and PF4 are critical for high-level neutrophil-activating function. Desensitization studies provided information on receptor binding. NAP- 2, which binds almost exclusively to the type 2 IL-8 receptor (IL-8R), did not desensitize neutrophils to activation by IL-8 because IL-8 could bind to and activate via both type 1 and 2 IL-8R. AELR/PF4 appears to bind to both types of receptors because it desensitized neutrophils to NAP-2 activation; but was not desensitized by NAP-2, and because it desensitized to and was desensitized by IL-8. Thus, although NAP-2 and AELR/PF4 share approximately 60% amino acid homology, they have different receptor affinities. Studies were performed to define the role of the C-termini of these platelet chemokines in receptor binding. Heparin and a monoclonal antibody specific for the heparin- binding domain of PF4 both inhibited Ca2+ mobilization and elastase release, further suggesting that the C-terminus of these chemokines is important in receptor binding. Synthetic NAP-2(51-70) failed to mobilize Ca2+, whereas PF4(47-70) and PF4(58-70) induced Ca2+ mobilization and secretion of elastase at high concentrations. Pertussis toxin inhibited neutrophil activation by 40% to 50%, establishing a role for G-protein-coupled receptors such as the IL-8Rs in activation by the PF4 C-terminal peptides.(ABSTRACT TRUNCATED AT 400 WORDS)  相似文献   
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